Cardiovascular disease, including atherosclerosis, is the leading cause of death in the United States. The medical community has developed a number of methods for treatment of coronary heart disease, some of which are specifically designed to treat complications resulting from atherosclerosis and other forms of coronary arterial narrowing.
In another form, arterial wall degeneration with the formation of aneurysms causes arterial wall thinning. Management of the dilated arteries in the peripheral circulation has come under the domain of vascular surgeons.
Investigators in the field of vascular surgery had at one time handled both narrowed and dilated arteries by techniques for suture anastomosis (sewing together) of two arterial segments using needle and thread. Today, there is a significantly less invasive clinical approach known as endovascular grafting.
However, the most compelling development in the past decade is percutaneous transluminal coronary angioplasty (PTCA, or simply "angioplasty"). The objective in angioplasty is to enlarge the lumen of the affected coronary artery by radial hydraulic expansion. The procedure is accomplished by inflating a balloon within the narrowed lumen of the coronary artery. Radial expansion of the coronary artery occurs in several different dimensions and is related to the nature of the plaque. Soft, fatty plaque deposits are flattened by the balloon and hardened deposits are cracked and split to enlarge the lumen. The wall of the artery itself is stretched when the balloon is inflated.
PTCA is performed as follows: A thin walled, hollow guiding catheter is typically introduced into the body via a relatively large vessel, such as the femoral artery in the groin area or the brachial artery in the arm. Access to the femoral artery is achieved by introducing a large bore needle directly into the femoral artery, a procedure known as the Seldinger technique. Once access to the femoral artery is achieved, a short hollow sheath is introduced to maintain a passageway during PTCA. The flexible guiding catheter, which is typically polymer coated, and lined with Teflon.TM., is inserted through the sheath into the femoral artery. The guiding catheter is advanced through the femoral artery into the iliac artery and into the ascending aorta. Further advancement of the flexible catheter involves the negotiation of an approximately 180 degree turn through the aortic arch to allow the guiding catheter to descend into the aortic cusp where entry may be gained to either the left or the right coronary artery as desired.
After the guiding catheter is advanced to the ostium of the coronary artery to be treated by PTCA, a flexible guidewire is inserted into the guiding catheter through a balloon and advanced to the area to be treated. The guide wire provides the necessary steerability for lesion passage. The guidewire is advanced across the lesion, or "wires" the lesion, in preparation for the advancement of the balloon catheter across the guide wire. The balloon, or dilatation, catheter is placed in position by sliding it along the guide wire. The use of a relatively rigid guide wire is necessary to advance the catheter through the narrowed lumen of the artery and to direct the balloon, which is typically quite flexible, across the lesion. Radiopaque markers in the balloon segments of the catheter facilitate positioning across the lesion. The balloon catheter is then inflated with contrast material to permit fluoroscopic viewing during treatment. The balloon is alternately inflated and deflated until the lumen of the artery is satisfactory enlarged.
By way of example, further details of angioplasty procedures and devices used in such procedures can be found in U.S. Pat. No. 4,327,071 (Simpson et al.), U.S. Pat. No. 4,332,254 (Lundquist), U.S. Pat. No. 4,439,185 (Lundquist), U.S. Pat. No. 4,468,224 (Enzmann et al.), U.S. Pat. No. 4,516,972 (Samson), U.S. Pat. No. 4,582,181 (Samson), U.S. Pat. No. 4,748,982 (Horzewski et al.), U.S. Pat. No. 4,771,778 (Mar), and U.S. Pat. No. 4,793,350 (Mar et al.), each of which is hereby incorporated by reference herein.
A common problem that sometimes occurs after an angioplasty procedure is the appearance of restenosis at or near the site of the original stenosis in the blood vessel, which requires a secondary angioplasty procedure or bypass surgery. Another occurrence which reduces the success of angioplasty procedures is the collapse of a section of the dissected lining (commonly termed a "flap") into the blood stream upon deflation of the balloon, thereby closing or significantly reducing the blood flow through the vessel. In this instance, emergency bypass surgery is sometimes required to avoid a myocardial infarct distal blockage.
On some occasions, the dilatation catheter can be replaced with a perfusion type dilatation catheter such as described in U.S. Pat. No. 4,790,315 (Mueller, Jr. et al.) in order to hold the blood vessel open for extended periods. However, perfusion type dilatation catheters have relatively large profiles which can make advancement thereof through the blockage difficult, and therefore immediate bypass surgery may be the only means of avoiding an infarct distal to the blockage or possibly even death. Additionally, the inflated balloon of these perfusion catheters can block off a branch artery, thus creating ischemic conditions in the side branch distal to the blockage.
In recent years, various devices and methods for prevention of restenosis and repairing damaged blood vessels have been developed which typically use an expandable cage or region commonly termed a "stent" which is placed on the distal end of a catheter, and is designed to hold a detached lining against an arterial wall for extended periods to facilitate the reattachment thereof. Stents are generally cylindrically shaped intravascular devices which in some cases can also be used as the primary treatment devices where they are expanded to dilate a stenosis and then left in place.
Various types of stents and stent delivery systems are disclosed in U.S. Pat. No. 3,868,956 (Alfidi et al.), U.S. Pat. No. 4,503,569 (Dotter), U.S. Pat. No. 4,512,338 (Balko et al.), U.S. Pat. No. 4,553,545 (Maass et al.), U.S. Pat. No. 4,655,771 (Wallsten), U.S. Pat. No. 4,665,918 (Garza et al.), U.S. Pat. No. 4,733,665 (Palmaz), U.S. Pat. No. 4,795,458 (Regan), U.S. Pat. No. 4,800,882 (Gianturco), U.S. Pat. No. 4,830,003 (Wolff et al.), U.S. Pat. No. 4,856,516 (Hillstead), U.S. Pat. No. 4,878,906 (Lindemann et al.), U.S. Pat. No. 4,886,062 (Wiktor), U.S. Pat. No. 4,907,336 (Gianturco), U.S. Pat. No. 5,201,757 (Heyn et al.), U.S. Pat. No. 5,234,457 (Andersen), U.S. Pat. No. 5,292,331 (Boneau), U.S. Pat. No. 5,314,444 (Gianturco), U.S. Pat. No. 5,344,426 (Lau et al.), U.S. Pat. No. 5,372,600 (Beyar et al.), U.S. Pat. No. 5,387,235 (Chuter), U.S. Pat. No. 5,449,373 (Pinchasik et al.), U.S. Pat. No. 5,540,712 (Kleshinski et al.), U.S. Pat. No. 5,549,662 (Fordenbacher), U.S. Pat. No. 5,591,197 (Orth et al.), U.S. Pat. No. 5,593,434 (Williams), U.S. Pat. No. 5,599,576 (Opolski), U.S. Pat. No. 5,607,467 (Froix), U.S. Pat. No. 5,603,721 (Lau et al.), U.S. Pat. No. 5,605,530 (Fischell et al.), U.S. Pat. No. 5,382,261 (Palmaz), U.S. Pat. No. 5,549,635 (Solar), U.S. Pat. No. 5,500,013 (Buscemi et al.), U.S. Pat. No. 5,234,456 (Silvestrini), U.S. Pat. No. 5,342,348 (Kaplan), U.S. Pat. No. 5,368,566 (Crocker), U.S. Pat. No. 5,383,928 (Scott et al.), U.S. Pat. No. 5,423,885 (Williams), U.S. Pat. No. 5,443,458 (Eury), U.S. Pat. No. 5,464,450 (Buscemi et al.), U.S. Pat. No. 5,464,650 (Berg et al.), U.S. Pat. No. 5,618,299 (Khosravi et al.), U.S. Pat. No. 5,637,113 (Tartaglia et al.), U.S. Pat. No. 5,649,977 (Campbell), U.S. Pat. No. 5,419,760 (Narciso, Jr.), U.S. Pat. No. 5,651,174 (Schwartz et al.), and U.S. Pat. No. 5,556,413 (Lam), each of which is hereby incorporated by reference herein. See especially U.S. Pat. No. 4,800,882 to Gianturco, U.S. Pat. No. 5,234,457 to Andersen, U.S. Pat. No. 4,856,516 to Hillstead, and U.S. Pat. No. 5,500,013 to Buscemi et al.
Because it is of utmost importance to avoid thrombosis of the stent and its serious complications, patients who receive stents are often aggressively treated with anticoagulants such as heparin, aspirin, coumadin, dextran, and/or persantine. As expected, there is a high incidence of bleeding complications in these patients. A study performed at Emory University Hospital revealed that 33% of the patients who received stents for acute closure required transfusion, and 7% of the patients had an extremely large bleeding episode at the catheter entry site in the leg artery that necessitated surgical repair (Hearn et al., J. Am. Coll. Cardiol., (1992).
Because of the complications associated with systemic treatment with anticoagulants, extensive attempts have been made to desing a stent that would be non-thrombogenic. A stent with little or no propensity to form thrombus would drastically decrease the need for aggressive treatment with anticoagulants. Initially, stents were constructed of plastic. Because all of these stents caused thrombosis, stainless steel was then tried. These stents appeared promising in studies in canine peripheral arteries. However, most coronary stents used to date in clinical trials are composed of stainless steel and yet still have a thrombotic occlusion rate of approximately 5-30%. Tantalum is another metal that is used in stents. Although initial reports of a lower thrombogenicity of tantalum stents appeared promising (van der Giessen et al., Circulation, 80:II-173 (1989)), more careful study has shown that tantalum is as thrombogenic as stainless steel (de Jaegere et al., Amer. J. Cardiol., 69:598-602 (1992)).
The concept of coating a stent with a polymer was described several years ago and is discussed in the literature regularly. In the past, local delivery of drug(s) using stents has centered around two concepts: (1) directly coating the stent wires with a drug or a drug-polymer combination (Bailey et al., Circulation, 82:III-541 (1990); and Cavendar et al., Circulation, 82:III-541 (1990)); and (2) incorporating a drug into a stent that is constructed of a biodegradable polymer (Murphy et al., J. Invasive Cardiol., 3:144-48 (1991)). Most investigators and stent companies have focussed their efforts on directly coating the metal stent wires with a polymer. This polymer is usually placed directly on the stent (e.g., by dipping the stent in soluble polymer) or is covalently bound to the metal. The polymer is bonded to or contains an anticoagulant compound most coated stents currently under development use heparin as their active agent. One of the more effective polymer coatings for stents is Biogold (van der Giessen, Circulation, 82:III-542 (1990)).
Significant difficulties have been encountered with all prior art stents. Each has its percentage of thrombosis, restenosis, and tissue in-growth problems, as well as various degrees of difficulty of deployment. Another difficulty is that many prior art stents do not conform well to the vessel lumen. Some prior art stents require administration of anticoagulant medication to the patient for up to three months following their placement inside the body. What has been needed and heretofore unavailable in the art is a stent that can be quickly and easily used in a wide variety of situations, that keeps the vessel open with a minimum degree of recoil and shortening lengthwise, that is flexible and can be delivered to the most distal lesion, and that can continuously deliver anticoagulant or other biologically active agents for an extended period directly at the site of stent placement.